Myocardial infarctions are one of the leading causes of death in the United States. As reported in Harrison, Principles of Internal Medicine (12th Ed. 1991) Vol. 1 at 953, approximately 1.5 million myocardial infarctions are reported to occur each year in the United States, alone. As much as 25 percent of persons suffering an acute myocardial infarction have been reported to die shortly after the episode. Of those 25 percent, about half die before reaching a hospital.
The mortality rate from myocardial infarction tells only part of the story, however. For every person that dies of a myocardial infarction, three persons survive their episode. A large portion of the survivors sustain irreversible damage to their heart muscle leaving them with reduced cardiac function. This disability decreases their quality of life and their life expectancy, and is a major contributor to the cost of health care in the United States and other countries.
Myocardial infarctions cause death and disability by two primary mechanisms. First, damaged heart muscle is subject to a variety of electrical disturbances collectively known as "arrhythmias." These arrhythmias can cause sudden death, syncopal episodes or lead to ischemic episodes in other organs including the brain. Secondly, damaged heart muscle does not regenerate to any appreciable degree (unlike skin or liver tissue) such that dead heart muscle permanently looses its contractile nature. As the heart looses its ability to contract, the person becomes more restricted in his activities of daily living. At some degree of loss, depending on the location of the dead muscle, the heart will pass a critical point leading to pump failure and death.
Myocardial infarctions have several known causes. Most commonly, they are the result of vasospastic episodes in the coronary arteries, emboli to the coronary arteries, thrombi in the coronary arteries, or a combination of vasospasm, emboli and thrombi. Two of the three common causes, emboli and thrombi, are clots formed to varying degrees of cells and cellular debris, platelets, products of the coagulation system, and cholesterol, triglycerides and other fats.
The ideal management for myocardial infarctions is prevention. There is major ongoing research into methods of prevention and there has been significant progress in decreasing the incidence of myocardial infarction in recent years. However, treatment of myocardial infarctions once they have occurred is still a mainstay of management.
Traditionally, treatment of myocardial infarctions took the form of bed rest, oxygen and analgesics. More recently, invasive and non-invasive monitoring combined with effective anti-arrhythmics have decreased the rates of morbidity and mortality. Further, drugs have been developed which alter vascular tone and the contractile state of the remaining normal heart muscle to prevent and treat pump failure.
One recent advance in treatment has been attempt to restore vascular patency in the occluded arteries. This has been done by surgical means through coronary artery bypass grafting, mainly in situations where occlusion was imminent but not complete. Similarly, percutaneous transluminal coronary angioplasty has been performed in such situations using balloons, burrs and lasers. In addition, some progress has been made with various drug therapy approaches, using drugs which dissolve products of the coagulation system, sometimes referred to as "thrombolytic" drugs.
A variety of efforts have been made to design catheters for delivering thrombolytic or other intravascular drugs. For example, U.S. Pat. No. 5,087,244 to Wolinsky et al. discloses a catheter having a perforated inflatable balloon for expressing drug to the vascular wall. U.S. Pat. No. 5,021,044 to Sharkawy discloses an infusion catheter having a plurality of effluent flow ports along its outer wall, each having a successively larger diameter in the distal direction.
U.S. Pat. No. 4,968,307 to Dake et al. discloses another catheter for infusion of therapeutic fluids, in which each effluent flow port through the wall of the catheter is placed in fluid communication with a fluid source by a unique flow passageway extending throughout the length of and within the wall of the catheter body.
Notwithstanding the foregoing, there remains a need for a low profile infusion catheter for delivering thrombolytic drugs to a preselected site, with improved flexibility characteristics and relatively uniform delivery over a preselected axial length.